Heat Stress (heat + stress)

Distribution by Scientific Domains
Distribution within Life Sciences


Selected Abstracts


Exercise Heat Stress does not Reduce Central Activation to non-exercised Human Skeletal Muscle

EXPERIMENTAL PHYSIOLOGY, Issue 6 2003
Julian Saboisky
In this study we measured the central activation ratio (CAR) of the leg extensors and the elbow flexor muscles before and after exhaustive exercise in the heat to determine whether exercise-induced hyperthermia affects the CNS drive to exercised (leg extensors) and/or non-exercised (forearm flexors) muscle groups. Thirteen subjects exercised at fixed intensities representative of a percentage of peak power output (PPO) for 10 min periods (50%, 40%, 60%, 50%) and then at 75% PPO until exhaustion in ambient conditions of 39.3 ± 0.8 °C and 60.0 ± 0.8% relative humidity. Before and immediately following exercise subjects performed a series of maximal voluntary contractions (MVCs) with the leg extensors (exercised muscles) and forearm flexors (non-exercised muscles). The degree of voluntary activation during the sustained MVCs was assessed by superimposing electrical stimulation to the femoral nerve and the biceps brachii. Exercise to exhaustion increased the rectal temperature from 37.2 ± 0.2 to 38.8 ± 0.2 °C (P < 0.0001). The mean heart rate at the end of exercise to exhaustion was 192 ± 3 beats min,1. Leg extensor voluntary force was significantly reduced from 595 ± 143 to 509 ± 105 N following exercise-induced hyperthermia but forearm flexor force was similar before and after exercise. The CAR of the leg extensors decreased from 94.2 ± 1.3% before exercise to 91.7 ± 1.5% (P < 0.02) following exercise-induced hyperthermia. However, the CAR for the forearm flexors remained at similar levels before and after exercise. The data suggest that the central nervous system selectively reduces central activation to specific skeletal muscles as a consequence of exercise-induced hyperthermia. [source]


Wheat Cellular Membrane Thermotolerance Under Heat Stress

JOURNAL OF AGRONOMY AND CROP SCIENCE, Issue 2 2010
A. S. Dias
Abstract Four genotypes of Triticum aestivum L. and Triticum turgidum subsp. durum chosen according to their genetic background diversity were subjected to heat stress after anthesis. Membrane permeability, lipid peroxidation and fatty acids (C14:0, C16:0, C16:1c, C16:1t, C18:0, C18:1, C18:2 and C18:3) were quantified. The estimation of the quantum yield of non-cyclic photosynthetic electron transport was used as well as a test system to further evaluate the implications on thylakoid functioning. It was found differences within bread and durum wheat species concerning the capability to cope with high temperatures at the stage of grain filling. The genotype Sever showed high thermal sensitivity concerning membrane lipid peroxidation and membrane permeability, as evaluated by the increased production of ethylene and MDA, as well as by the impact on TFA (at the middle term of grain filling). In the durum wheat genotypes, differences were also found, with TE 9306 displaying high membrane stability, with no increases on membrane permeability, MDA and ethylene content. In this way, the observed changes on TFA in this genotype might have constituted a mechanism to allow qualitative lipid changes, reflected in lower unsaturation level of membrane FAs which is a positive trait under high temperatures. [source]


Cardiovascular function in the heat-stressed human

ACTA PHYSIOLOGICA, Issue 4 2010
C. G. Crandall
Abstract Heat stress, whether passive (i.e. exposure to elevated environmental temperatures) or via exercise, results in pronounced cardiovascular adjustments that are necessary for adequate temperature regulation as well as perfusion of the exercising muscle, heart and brain. The available data suggest that generally during passive heat stress baroreflex control of heart rate and sympathetic nerve activity are unchanged, while baroreflex control of systemic vascular resistance may be impaired perhaps due to attenuated vasoconstrictor responsiveness of the cutaneous circulation. Heat stress improves left ventricular systolic function, evidenced by increased cardiac contractility, thereby maintaining stroke volume despite large reductions in ventricular filling pressures. Heat stress-induced reductions in cerebral perfusion likely contribute to the recognized effect of this thermal condition in reducing orthostatic tolerance, although the mechanism(s) by which this occurs is not completely understood. The combination of intense whole-body exercise and environmental heat stress or dehydration-induced hyperthermia results in significant cardiovascular strain prior to exhaustion, which is characterized by reductions in cardiac output, stroke volume, arterial pressure and blood flow to the brain, skin and exercising muscle. These alterations in cardiovascular function and regulation late in heat stress/dehydration exercise might involve the interplay of both local and central reflexes, the contribution of which is presently unresolved. [source]


Drought stress effects on photosystem I content and photosystem II thermotolerance analyzed using Chl a fluorescence kinetics in barley varieties differing in their drought tolerance

PHYSIOLOGIA PLANTARUM, Issue 2 2009
Abdallah Oukarroum
Drought stress has multiple effects on the photosynthetic system. Here, we show that a decrease of the relative contribution of the I-P phase, ,VIP = ,VI = (FM,FI)/(FM, Fo), to the fluorescence transient OJIP is observed in 10 drought-stressed barley and 9 chickpea varieties. The extent of the I-P loss in the barley varieties depended on their drought tolerance. The relative loss of the I-P phase seems to be related to a loss of photosystem (PS) I reaction centers as determined by 820-nm transmission measurements. In the second part of this study, the interaction of drought and heat stress in two barley varieties (the drought tolerant variety A¨t Baha and the drought sensitive variety Lannaceur) was studied using a new approach. Heat stress was induced by exposing the plant leaves to temperatures of 25,45°C and the inactivation of the O2 -evolving complex (OEC) was followed measuring chlorophyll a (Chl a) fluorescence using a protocol consisting of two 5-ms pulses spaced 2.3 ms apart. In active reaction centers, the dark interval is long enough to allow the OEC to recover from the first pulse; whereas in heat-inactivated reaction centers it is not. In the latter category of reaction centers, no further fluorescence rise is induced by the second pulse. Lannaceur, under well-watered conditions, was more heat tolerant than Aït Baha. However, this difference was lost following drought stress. Drought stress considerably increased the thermostability of PS II of both varieties. [source]


Heat stress activates phospholipase D and triggers PIP2 accumulation at the plasma membrane and nucleus

THE PLANT JOURNAL, Issue 1 2009
Michael Mishkind
Summary Heat stress induces an array of physiological adjustments that facilitate continued homeostasis and survival during periods of elevated temperatures. Here, we report that within minutes of a sudden temperature increase, plants deploy specific phospholipids to specific intracellular locations: phospholipase D (PLD) and a phosphatidylinositolphosphate kinase (PIPK) are activated, and phosphatidic acid (PA) and phosphatidylinositol 4,5-bisphosphate (PIP2) rapidly accumulate, with the heat-induced PIP2 localized to the plasma membrane, nuclear envelope, nucleolus and punctate cytoplasmic structures. Increases in the steady-state levels of PA and PIP2 occur within several minutes of temperature increases from ambient levels of 20,25°C to 35°C and above. Similar patterns were observed in heat-stressed Arabidopsis seedlings and rice leaves. The PA that accumulates in response to temperature increases results in large part from the activation of PLD rather than the sequential action of phospholipase C and diacylglycerol kinase, the alternative pathway used to produce this lipid. Pulse-labelling analysis revealed that the PIP2 response is due to the activation of a PIPK rather than inhibition of a lipase or a PIP2 phosphatase. Inhibitor experiments suggest that the PIP2 response requires signalling through a G-protein, as aluminium fluoride blocks heat-induced PIP2 increases. These results are discussed in the context of the diverse cellular roles played by PIP2 and PA, including regulation of ion channels and the cytoskeleton. [source]


Identification of novel heat shock factor-dependent genes and biochemical pathways in Arabidopsis thaliana

THE PLANT JOURNAL, Issue 1 2005
Wolfgang Busch
Summary In order to assess specific functional roles of plant heat shock transcription factors (HSF) we conducted a transcriptome analysis of Arabidopsis thaliana hsfA1a/hsfA1b double knock out mutants and wild-type plants. We used Affymetrix ATH1 microarrays (representing more than 24 000 genes) and conducted hybridizations for heat-treated or non-heat-treated leaf material of the respective lines. Heat stress had a severe impact on the transcriptome of mutant and wild-type plants. Approximately 11% of all monitored genes of the wild type showed a significant effect upon heat stress treatment. The difference in heat stress-induced gene expression between mutant and wild type revealed a number of HsfA1a/1b-regulated genes. Besides several heat shock protein and other stress-related genes, we found HSFA-1a/1b-regulated genes for other functions including protein biosynthesis and processing, signalling, metabolism and transport. By screening the profiling data for genes in biochemical pathways in which known HSF targets were involved, we discovered that at each step in the pathway leading to osmolytes, the expression of genes is regulated by heat stress and in several cases by HSF. Our results document that in the immediate early phase of the heat shock response HSF-dependent gene expression is not limited to known stress genes, which are involved in protection from proteotoxic effects. HsfA1a and HsfA1b-regulated gene expression also affects other pathways and mechanisms dealing with a broader range of physiological adaptations to stress. [source]


The effect of high ambient temperature on Ca, P and Mg balance and bone turnover in high-yielding dairy cows

ANIMAL SCIENCE JOURNAL, Issue 4 2010
Yuko KAMIYA
ABSTRACT We investigated the effect of heat stress on Ca, P and Mg balance and bone turnover in lactating cows. In a 2 × 2 crossover design, four multiparous lactating Holstein cows were kept in a chamber and subjected to a constant moderate (18°C) ambient temperature (MT) or high (28°C) ambient temperature (HT). The cows were fed total mixed ration (Ca, 0.7%; P, 0.4%; Mg, 0.2%) ad libitum. The milk yield under HT (35.4 kg/day) tended to be lower (P < 0.10) than that under MT (43.2 kg/day). The concentrations of milk P (P < 0.05) and Mg (P < 0.01) were significantly lower under HT than MT. The Ca, P and Mg intake (P < 0.10); Ca (P < 0.10), P, and Mg (P < 0.05) secretion into milk; and Ca (P < 0.05), P (P < 0.01), and Mg (P < 0.05) absorption in the intestine were lower under HT than MT. The plasma osteocalcin, a marker of bone turnover, was significantly lower (P < 0.05) under HT than MT. Heat stress did not affect plasma C-telopeptide of collagen type I, a bone resorption marker, and plasma parathyroid hormone concentration. [source]


NEW INSIGHT INTO THE SIGNALLING PATHWAYS OF HEAT STRESS-INDUCED MYOCARDIAL PRECONDITIONING: PROTEIN KINASE C, TRANSLOCATION AND HEAT SHOCK PROTEIN 27 PHOSPHORYLATION

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 3 2004
Claire Arnaud
SUMMARY 1.,Heat stress (HS) is known to induce delayed preconditioning against myocardial infarction 24 h later, but the exact signalling pathway of this response remains to be elucidated. In previous studies, we have shown evidence for the implication of protein kinase C (PKC) and p38 mitogen-activated protein kinase (MAPK) in the HS-induced reduction in infarct size. Furthermore, in their phosphorylated state, small heat shock proteins (Hsp27) seem to confer cytoskeletal protection. In the present study, we sought to determine the effect of HS on the subcellular distribution of PKC isoforms and on Hsp27 phosphorylation. 2.,Rats were subjected to either HS (42°C for 15 min; HS group) or sham anaesthesia (sham group) before their hearts were excised. Myocardial tissue extracts obtained 20 min or 24 h after HS were processed for western blot analysis. 3.,In the HS group, PKC, translocated from the cytosolic to the particulate fraction (4426 ± 128 vs 6258 ± 316 arbitrary units; P = 0.002). Chelerythrine (5 mg/kg, i.p.), a PKC inhibitor, abolished this translocation. Western blot analysis of Hsp27 24 h after HS showed a marked increase in protein expression and phosphorylation in the particulate fraction. 4.,In the present study, we have shown that HS induces the translocation of PKC, from the cytosolic to the particulate fraction. Along with our previous observation that PKC is a trigger of HS-induced myocardial preconditioning, the results of the present study suggest an important role of the , isoform of PKC in this cardioprotective mechanism. Furthermore, we have also demonstrated that the cytoprotective protein Hsp27 is phosphorylated following HS. Therefore, we can conclude that PKC and MAPK/Hsp27 are involved in the signalling pathway of HS-induced cardioprotection. [source]


Heat stress increases endothelium-dependent relaxations and prevents reperfusion-induced endothelial dysfunction

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 11 2002
Vincent Richard
Summary 1.,Heat stress has been widely used to stimulate the expression of stress proteins and is associated with various cardiovascular changes, including anti-ischaemic effects. However, the effect of heat stress on endothelial function is less clear. 2.,Heat stress was induced in anaesthetized rats by increasing body temperature to 42°C for 15 min. Twenty-four hours later, segments of rat aorta and mesenteric and coronary arteries were mounted in organ chambers. 3.,Heat stress markedly increased relaxation to acetylcholine (ACh) in all three blood vessels studied, without affecting the response to the nitric oxide (NO) donor sydnonimine-1. 4.,Heat stress also increased aortic relaxation to histamine and the calcium ionophore A23187. 5.,In the aorta, an inhibitor of NO synthesis abolished the response to ACh in both control and heat stressed-rings, whereas a cyclo-oxygenase inhibitor had no effect. 6.,Heat stress also prevented completely the impaired response to ACh in coronary arteries isolated from rats subjected to myocardial ischaemia and reperfusion. 7.,Thus, heat stress increases the stimulated release of NO the rat aorta and mesenteric and coronary arteries and prevents reperfusion-induced injury at the level of the coronary endothelium. [source]


Cardiovascular function in the heat-stressed human

ACTA PHYSIOLOGICA, Issue 4 2010
C. G. Crandall
Abstract Heat stress, whether passive (i.e. exposure to elevated environmental temperatures) or via exercise, results in pronounced cardiovascular adjustments that are necessary for adequate temperature regulation as well as perfusion of the exercising muscle, heart and brain. The available data suggest that generally during passive heat stress baroreflex control of heart rate and sympathetic nerve activity are unchanged, while baroreflex control of systemic vascular resistance may be impaired perhaps due to attenuated vasoconstrictor responsiveness of the cutaneous circulation. Heat stress improves left ventricular systolic function, evidenced by increased cardiac contractility, thereby maintaining stroke volume despite large reductions in ventricular filling pressures. Heat stress-induced reductions in cerebral perfusion likely contribute to the recognized effect of this thermal condition in reducing orthostatic tolerance, although the mechanism(s) by which this occurs is not completely understood. The combination of intense whole-body exercise and environmental heat stress or dehydration-induced hyperthermia results in significant cardiovascular strain prior to exhaustion, which is characterized by reductions in cardiac output, stroke volume, arterial pressure and blood flow to the brain, skin and exercising muscle. These alterations in cardiovascular function and regulation late in heat stress/dehydration exercise might involve the interplay of both local and central reflexes, the contribution of which is presently unresolved. [source]


Cerebral oxygenation is reduced during hyperthermic exercise in humans

ACTA PHYSIOLOGICA, Issue 1 2010
P. Rasmussen
Abstract Aim:, Cerebral mitochondrial oxygen tension (PmitoO2) is elevated during moderate exercise, while it is reduced when exercise becomes strenuous, reflecting an elevated cerebral metabolic rate for oxygen (CMRO2) combined with hyperventilation-induced attenuation of cerebral blood flow (CBF). Heat stress challenges exercise capacity as expressed by increased rating of perceived exertion (RPE). Methods:, This study evaluated the effect of heat stress during exercise on PmitoO2 calculated based on a Kety-Schmidt-determined CBF and the arterial-to-jugular venous oxygen differences in eight males [27 ± 6 years (mean ± SD) and maximal oxygen uptake (VO2max) 63 ± 6 mL kg,1 min,1]. Results:, The CBF, CMRO2 and PmitoO2 remained stable during 1 h of moderate cycling (170 ± 11 W, ,50% of VO2max, RPE 9,12) in normothermia (core temperature of 37.8 ± 0.4 °C). In contrast, when hyperthermia was provoked by dressing the subjects in watertight clothing during exercise (core temperature 39.5 ± 0.2 °C), PmitoO2 declined by 4.8 ± 3.8 mmHg (P < 0.05 compared to normothermia) because CMRO2 increased by 8 ± 7% at the same time as CBF was reduced by 15 ± 13% (P < 0.05). During exercise with heat stress, RPE increased to 19 (19,20; P < 0.05); the RPE correlated inversely with PmitoO2 (r2 = 0.42, P < 0.05). Conclusion:, These data indicate that strenuous exercise in the heat lowers cerebral PmitoO2, and that exercise capacity in this condition may be dependent on maintained cerebral oxygenation. [source]


Stress Resistance and Environmental Dependency of Inbreeding Depression in Drosophila melanogaster

CONSERVATION BIOLOGY, Issue 4 2000
Jesper Dahlgaard
Two important issues are whether stress and inbreeding effects are independent as opposed to synergistic, and whether inbreeding effects are general across stresses as opposed to stress-specific. We found that inbreeding reduced resistance to acetone and desiccation in adult Drosophila melanogaster, whereas resistance to knockdown heat stress was not affected. Inbred flies, however, experienced a greater proportional decrease in productivity than outbreds following heat stress. Correlations using line means indicated that all resistance traits were uncorrelated in the inbred as well as in the outbred flies. Recessive, deleterious alleles therefore did not appear to have any general deleterious effects on stress resistance. Inbreeding within a specific environment and selection for resistant genotypes may therefore purge a population of deleterious genes specific to only one environmental stress. Resumen: Tanto la endogamia como el estrés ambiental pueden tener efectos adversos sobre la adaptabilidad afectando la conservación de especies en peligro de extinción. Dos temas importantes son determinar si los efectos del estrés y la endogamia son independientes en lugar de ser sinérgicos, y determinar si los efectos de la endogamia son generales para distintos tipos de estrés o si son específicos para un tipo determinado de estrés. Encontramos que la endogamia reduce la resistencia a la acetona y la desecación en adultos de Drosophila melanogaster, mientras que la resistencia al efecto demoledor del estrés por calor no fue afectada. Sin embargo, las moscas endogámicas experimentaron una disminución proporcionalmente mayor en la productividad que aquellas moscas sin endogamia después de experimentar un estrés por calor. Las correlaciones obtenidas usando líneas medias indicaron que las características de resistencia no estuvieron correlacionadas ni en moscas con endogamia, ni en moscas sin ella. Aparentemente los alelos nocivos recesivos no tuvieron ningún efecto nocivo general en la resistencia al estrés. La endogamia dentro de un ambiente específico y la selección por genotipos resistentes podrían, por lo tanto, eliminar una población de genes nocivos específicos a un solo estrés ambiental. [source]


AN INTERSPECIFIC TEST OF ALLEN'S RULE: EVOLUTIONARY IMPLICATIONS FOR ENDOTHERMIC SPECIES

EVOLUTION, Issue 12 2007
R. L. Nudds
Ecogeographical rules provide potential to describe how organisms are morphologically constrained to climatic conditions. Allen's rule (relatively shorter appendages in colder environments) remains largely unsupported and there remains much controversy whether reduced surface area of appendages provides energetic savings sufficient to make this morphological trend truly adaptive. By showing for the first time that Allen's rule holds for closely related endothermic species, we provide persuasive support of the adaptive significance of this trend for multiple species. Our results indicate that reduction of thermoregulatory cost during the coldest part of the breeding season is the most likely mechanism driving Allen's rule for these species. Because for 54% of seabird species examined, rise in seasonal maximum temperature over 100 years will exceed that for minimum temperatures, an evolutionary mismatch will arise between selection for limb length reduction and ability to accommodate heat stress. [source]


Requirements for chromatin reassembly during transcriptional downregulation of a heat shock gene in Saccharomyces cerevisiae

FEBS JOURNAL, Issue 11 2008
Mette M. Jensen
Heat shock genes respond to moderate heat stress by a wave of transcription. The induction phase is accompanied by the massive eviction of histones, which later reassemble with DNA during the ensuing phase of transcription downregulation. In this article, we identify determinants of this reassembly throughout the heat shock protein 104 gene (HSP104) transcription unit. The results show that, although histone H3 lacking amino acids 4,30 of its N-terminal tail (H3,4,30) is normally deposited, reassembly of H3,4,40 is obliterated with an accompanying sustained transcription. On mutation of the histone chaperones Spt6p and Spt16p, but not Asf1p, reassociation of H3 with DNA is compromised. However, despite a lasting open chromatin structure, transcription ceases normally in the spt6 mutant. Thus, transcriptional downregulation can be uncoupled from histone redeposition and ongoing transcription is not required to prevent chromatin reassembly. [source]


Cloning and characterization of genes encoding trehalose-6-phosphate synthase (TPS1) and trehalose-6-phosphate phosphatase (TPS2) from Zygosaccharomyces rouxii

FEMS YEAST RESEARCH, Issue 4 2003
Hawk-Bin Kwon
Abstract In many organisms, trehalose protects against several environmental stresses, such as heat, desiccation, and salt, probably by stabilizing protein structures and lipid membranes. Trehalose synthesis in yeast is mediated by a complex of trehalose-6-phosphate synthase (TPS1) and trehalose-6-phosphate phosphatase (TPS2). In this study, genes encoding TPS1 and TPS2 were isolated from Zygosaccharomyces rouxii (designated ZrTPS1 and ZrTPS2, respectively). They were functionally identified by their complementation of the tps1 and tps2 yeast deletion mutants, which are unable to grow on glucose medium and with heat, respectively. Full-length ZrTPS1 cDNA is composed of 1476 nucleotides encoding a protein of 492 amino acids with a molecular mass of 56 kDa. ZrTPS2 cDNA consists of 2843 nucleotides with an open reading frame of 2700 bp, which encodes a polypeptide of 900 amino acids with a molecular mass of 104 kDa. The amino acid sequence encoded by ZrTPS1 has relatively high homology with TPS1 of Saccharomyces cerevisiae and Schizosaccharomyces pombe, compared with TPS2. Western blot analysis showed that the antibody against S. cerevisiae TPS1 recognizes ZrTPS1. Under normal growth conditions, ZrTPS1 and ZrTPS2 were highly and constitutively expressed, unlike S. cerevisiae TPS1 and TPS2. Salt stress and heat stress reduced the expression of the ZrTPS1 and ZrTPS2 genes, respectively. [source]


Looking for answers to questions about heat stress: researchers are getting warmer

FUNCTIONAL ECOLOGY, Issue 2 2009
Michael J. Angilletta Jr.
No abstract is available for this article. [source]


Integrated models of livestock systems for climate change studies.

GLOBAL CHANGE BIOLOGY, Issue 2 2001

Summary The potential impact of climate change by the year 2050 on intensive livestock systems in Britain is assessed through the use of simulation models of farming systems. The submodels comprise livestock feeding, livestock thermal balance and the thermal balance of controlled environment buildings and a stochastic weather generator. These are integrated to form system models for growing pigs and broiler chickens. They are applied to scenarios typical of SE England, which is the warmest region of the country and represents the worst case. For both species the frequency of severe heat stress is substantially increased, with a consequent risk of mortality. To offset this, it would be necessary to reduce stocking densities considerably, or to invest in improved ventilation or cooling equipment. Other effects on production are likely to be small. [source]


The effect of paternal heat stress on protein profiles of pre-implantation embryos in the mouse

INTERNATIONAL JOURNAL OF ANDROLOGY, Issue 3 2005
B. ZHU
Summary The study was undertaken to compare the protein profiles of [35S]-methionine-labelled control-sired embryos with heat-sired embryos at 7, 14 or 21 days after mature fertile B6CBF F1 male mice were kept at 36 ± 0.3 °C and 62 ± 2.7% relative humidity for 24 h. One-dimensional gel electrophoresis and autoradiographs were used to examine the protein profiles between the two-cell embryos and the blastocysts. The results obtained demonstrate that paternal heat stress 7 or 14 days earlier did not apparently affect protein patterns of two-cell embryos, four-cell to eight-cell embryos, morulae or blastocysts. However, 21 days earlier, there were changes in protein patterns of two-cell embryos and abnormal embryos, but not the morulae. To further support and extend these results, two-dimensional gel electrophoresis and phosphorimaging were employed and the results obtained show that paternal heat stress 21 days before mating affected protein profiles of two-cell embryos and morulae in the mouse. Together, these findings have indicated that paternal heat stress affects most but not all protein patterns of pre-implantation embryos, which strongly supports our previous results demonstrating that paternal heat stress significantly reduced the developmental proportion of pre-implantation embryos in the mouse. [source]


HtrA2 is up-regulated in the rat testis after experimental cryptorchidism

INTERNATIONAL JOURNAL OF UROLOGY, Issue 2 2006
TETSUO HAYASHI
Aim:, The aim of the present study was to elucidate the role of high temperature requirement A2 (HtrA2) in germ cell loss in the heat-stressed testis. Methods:, We examined the expression of HtrA2, caspase-9 activity and proteolytic activity of HtrA2 in the rat testis, and their in vivo responses to experimental cryptorchid treatment. Results:, Northern analysis revealed the expression of HtrA2 mRNA peaked at days 1 and 7 after cryptorchid treatment. While expression of HtrA2 mRNA was seen in the spermatogonium, spermatocytes and some spermatids in normal adult rat testis, experimental cryptorchidism treatment resulted in a marked increase in its signal intensity in spermatocytes and some spermatids, and the layers of spermatogonium and early primary spermatocytes became negative at days 1 and 7 after the treatment. However, the spermatogonium, Sertoli cells and interstitial cells appeared to have strong intensities at days 14, 28 and 56 after the treatment. Western analysis revealed the expression of HtrA2 protein peaked at day 2 coinciding with the increase of positive spermatogonium, the appearance of protein-positive interstitial cells, and day 28 coinciding with the reappearance of protein-positive interstitial cells. Caspase-9 activity peaked at day 2 and HtrA2 proteolytic activity peaked at day 28. Consequently, the first peak of HtrA2 mRNA expression was followed by the peak of caspase-9 activity and the second peak was followed by the peak of proteolytic activity; however, the second peak of mRNA expression had considerable chronological difference from that of the protein. Conclusion:, These findings suggest the probabilities that the heat stress results in germ cell death by a caspase-independent manner with the elevation of HtrA2 proteolytic activity, as well as a caspase-dependent manner with the elevation of caspase-9 activity. [source]


Heat Shock Protein in Developing Grains in Relation to Thermotolerance for Grain Growth in Wheat

JOURNAL OF AGRONOMY AND CROP SCIENCE, Issue 1 2010
P. Sharma-Natu
Abstract Wheat (Triticum aestivum L.) cvs DL 153-2 and HD 2285 (relatively tolerant), HD 2329 and WH 542 (relatively susceptible), were grown under normal (27 November) and late (28 December) sown conditions. In another experiment, these cultivars were grown under normal sowing and at anthesis stage, they were transferred to control (C) and heated (H) open top chambers (OTCs). Under late sowing, wheat cultivars were exposed to a mean maximum temperature of up to 3.6 °C higher than normal sowing and in H-OTCs, mean maximum temperature was 3.2 °C higher than C-OTCs during grain growth period. Heat susceptibility index (S) for grain growth and grain yield was determined at maturity in both the experiments. The level of heat shock protein (HSP 18) in the developing grains was determined in C- and H-OTC grown plants and in normal and late sown plants by Western blot analysis. The moderately high temperature exposure increased the accumulation of HSP 18 in the developing grains. The relatively tolerant cultivars, as also revealed from S, showed a greater increase in HSP 18 compared with susceptible types in response to moderate heat stress. An association of HSP 18 with thermotolerance for grain growth in wheat was indicated. [source]


Lack of Interaction between Extreme High-Temperature Events at Vegetative and Reproductive Growth Stages in Wheat

JOURNAL OF AGRONOMY AND CROP SCIENCE, Issue 3 2003
B. Wollenweber
Abstract Increased climatic variability and more frequent episodes of extreme conditions may result in crops being exposed to more than one extreme temperature event in a single growing season and could decrease crop yields to the same extent as changes in mean temperature. The developmental stage of the crop exposed to increased temperatures will determine the severity of possible damage experienced by the plant. It is not known whether or not the damaging effects of heat episodes occurring at different phenological stages are additive. In the present study, the interaction of high-temperature events applied at the stages of double ridges and anthesis in Triticum aestivum (L.) cv. Chablis was investigated. Biomass accumulation of control plants and that of plants experiencing high temperatures during the double-ridge stage were similar and were reduced by 40 % when plants were subjected to a heat event at anthesis. Grain number on the main and side tillers declined by 41 %, and individual grain weight declined by 45 % with heat stress applied at the double-ridge stage and anthesis or at anthesis alone. The harvest index was reduced from 0.53 to 0.33. Nitrogen contents in leaves were reduced by 10 % at the double-ridge stage and by 25 % at anthesis. The maximum rates of CO2 assimilation increased with heat stress at the double-ridge stage and higher rates were maintained throughout the growing season. The results clearly indicate that an extreme heat event at the double-ridge stage does not affect subsequent growth or the response of wheat to heat stress at anthesis. [source]


ORIGINAL ARTICLE: Ileal endogenous amino acid flow of broiler chickens under high ambient temperature

JOURNAL OF ANIMAL PHYSIOLOGY AND NUTRITION, Issue 5 2010
A. F. Soleimani
Summary High environmental temperature has detrimental effects on the gastrointestinal tract of poultry. An experiment was conducted to determine the effect of acute heat stress on endogenous amino acid (EAA) flow in broiler chickens. A total of 90, day-old broiler chicks were housed in battery cages in an environmentally controlled chamber. Chicks were fed a nitrogen-free diet on day 42 following either no heat exposure (no-heat) or 2 weeks exposure to 35 ± 1 °C for 3 h from days 28 to 42 (2-week heat) or 1 week exposure to 35 ± 1 °C for 3 h from days 35 to 42 (1 week heat). The most abundant amino acid in the ileal flow was glutamic acid, followed by aspartic acid, serine and threonine in non-heat stressed group. The EAA flow in 1-week heat and 2-week heat birds were significantly (p < 0.05) higher than those under no heat exposure (14682, 11161 and 9597 mg/kg of dry matter intake respectively). Moreover, the EAA flow of 2-week heat group was less than 1-week heat group by approximately 36%. These observations suggest that the effect of heat stress on EAA flow is mostly quantitative; however, heat stress may also alter the content of EAA flow qualitatively. [source]


Effects of vitamin E and selenium on performance, digestibility of nutrients, and carcass characteristics of Japanese quails reared under heat stress (34 °C)

JOURNAL OF ANIMAL PHYSIOLOGY AND NUTRITION, Issue 11-12 2001
K. Sahin
This study was conducted to determine the effects of vitamin E (dL-,-Tocopheryl acetate) and selenium (Se; Na2 -SeO3) on performance, digestibility of nutrients and carcass characteristics of Japanese quails reared under chronic heat stress (34 °C). A total of 120 10-day-old Japanese quails were randomly assigned to four treatment groups, three replicates of 10 birds each. The birds with a 2 × 2 factorial design received either two levels of vitamin E (125 and 250 mg/kg of diet) or two levels of Se (0.1 or 0.2 mg/kg of diet). A 250-mg vitamin E/kg of diet compared with that of 125 mg/kg of diet and higher dietary Se inclusions (0.1 vs. 0.2 mg/kg) resulted in a better performance (p=0.001). The interaction between vitamin E and Se for feed intake (p=0.03), final body weight change (p=0.03) and feed efficiency (p=0.001) was detected. Carcass yield increased with increasing both dietary vitamin E and Se (p=0.001). The interactions on carcass characteristics were all non-significant (p > 0.06). Digestibility of nutrients (DM, OM, CP and ether extract) was higher with higher dietary vitamin E (p=0.03), and DM digestibility was also higher with higher dietary Se (p=0.05). There were no interactions detected for digestibility of nutrients (p=0.28). From the results of the present study, it was concluded that a combination of 250 mg of vitamin E and 0.2 mg of Se provides the greatest performance in Japanese quails reared under heat stress and this combination can be considered as a protective management practice in Japanese quail diets, reducing the negative effects of heat stress. [source]


Effects of sequential exposure to lipopolysaccharide and heat stress on dental pulp cells

JOURNAL OF CELLULAR BIOCHEMISTRY, Issue 3 2006
Chiaki Kitamura
Abstract In the present study, we examined the effects of sequential exposure to bacterial lipopolysaccharide (LPS) and heat stress on dental pulp cells. LPS induced the proliferation of pulp cells through the activation of p38 MAPK. HSP27 was expressed in cells with or without LPS during the entire period of heat stress, while transiently phosphorylated by short-term heat stress. In LPS-treated cells, short-term heat stress also induced the phosphorylation of HSF1. The immediate phosphorylation of HSF1 and HSP27 in LPS-treated cells by short-term heat stress occurred dependent on the activation of p38 MAPK. However, with long-term heat stress, the activation of HSF1 and induction of HSP27 occurred independent of p38 MAPK. Further, full activation of Akt in LPS-treated cells was immediately induced by short-term heat stress and lasted during the entire period of heat stress. I,B, was induced and phosphorylated throughout sequential exposure to LPS and heat stress. These results suggest that LPS has the unique effects on the cytoprotection and the cell death of pulp cells during heat stress through the modification and the activation of heat stress responsive molecules, HSF1 and HSP27, and cell survival molecules, Akt and NF-,B/I,B,. J. Cell. Biochem. 99: 797,806, 2006. © 2006 Wiley-Liss, Inc. [source]


JNK phosphorylates the HSF1 transcriptional activation domain: Role of JNK in the regulation of the heat shock response

JOURNAL OF CELLULAR BIOCHEMISTRY, Issue 2 2001
Jeonghyeon Park
Abstract The role of c-Jun NH2 -terminal kinase (JNK) signaling cascade in the stress-inducible phosphorylation of heat shock factor 1 (HSF1) was investigated using known agonists and antagonists of JNK. We showed that treatment of HeLa cells with MG132, a proteasome inhibitor and known JNK activator, caused the transcriptional activation domain of HSF1 to be targeted and phosphorylated by JNK2 in vivo. Dose-response and time course studies of the effects of heat shock and anisomycin treatment showed a close correlation of the activation of JNK and hyperphosphorylation of HSF1. SB203580 inhibited JNK at the 100 ,M concentration and significantly reduced the amount of hyperphosphorylated HSF1 upon heat shock or anisomycin treatment. SB203580 and dominant-negative JNK suppress hsp70 promoter-driven reporter gene expression selectively at 45°C but not at 42°C heat stress, suggesting that JNK would be preferentially associated with the protective heat shock response against severe heat stress. The possibility that JNK-mediated phosphorylation of HSF1 may selectively stabilize the HSF1 protein and confers protection to cells under conditions of severe stress is discussed. J. Cell. Biochem. 82: 326,338, 2001. © 2001 Wiley-Liss, Inc. [source]


Reproductive value in a complex life cycle: heat tolerance of the pitcher-plant mosquito, Wyeomyia smithii

JOURNAL OF EVOLUTIONARY BIOLOGY, Issue 1 2005
P. A. Zani
Abstract Because mortality accumulates with age, Fisher proposed that the strength of selection acting on survival should increase from birth up to the age of first reproduction. Hamilton later theorized that the strength of selection acting on survival should not change from birth to age at first reproduction. As organisms in nature do not live in uniform environments but, rather, experience periodic stress, we hypothesized that resistance to environmental stress should increase (Fisher) or remain constant (Hamilton) from birth to age at first reproduction. Using the pitcher-plant mosquito, Wyeomyia smithii, we imposed heat stress by simulating the passage of a warm-weather front at different preadult and adult stages. Contrary to either Fisher or Hamilton, stress tolerance declined from embryos to larvae to pupae to adults. Consequently, reproductive value appears to have been of little consequence in the evolution of stage-specific tolerance of heat stress in W. smithii. [source]


Temperature-dependent changes in energy metabolism, intracellular pH and blood oxygen tension in the Atlantic cod

JOURNAL OF FISH BIOLOGY, Issue 6 2003
F. J. Sartoris
The effect of acute increase in temperature on oxygen partial pressure (Po2) was measured in the gill arches of Atlantic cod Gadus morhua between 10 and 19° C by use of oxygen microoptodes. Oxygen saturation of the gill blood under control conditions varied between 90 and 15% reflecting a variable percentage of arterial or venous blood in accordance with the position of each optode in the gill arch. The data obtained suggested that arterial Po2 remained more or less constant and arterial oxygen uptake did not become limiting during warming. A progressive drop in venous Po2, however, was observed at >10° C indicating that excessive oxygen uptake from the blood is not fully compensated for by circulatory performance, until finally, Po2 levels fully collapse. In a second set of experiments energy and acid,base status of white muscle of Atlantic cod in vivo was measured by magnetic resonance (31P-NMR) spectroscopy in unanaesthetized and unimmobilized fish in the temperature range between 13 and 21° C. A decrease in white muscle intracellular pH (pHi) with temperature occurred between 10 and 16° C (,pH per ° C = ,0·025 per ° C). In white muscle temperature changes had no influence on high-energy phosphates such as phosphocreatine (PCr) or ATP except during exposure to high critical temperatures (>16° C), indicating that white muscle energy status appears to be relatively insensitive to thermal stress if compared to the thermal sensitivity of the whole animal. The data were consistent with the hypothesis of an oxygen limitation of thermal tolerance in animals, which is set by limited capacity of oxygen supply mechanisms. In the case of Atlantic cod circulatory rather than ventilatory performance may be the first process to cause oxygen deficiency during heat stress. [source]


Hedging dairy production losses using weather-based index insurance

AGRICULTURAL ECONOMICS, Issue 2 2007
Xiaohui Deng
Dairy production risk; Index insurance; Temperature,humidity index Abstract This article proposes a temperature,humidity index insurance product and examines whether this product can effectively protect against the risk of reduced milk production caused by heat stress. Results suggest that even when premiums are at higher than actuarially fair levels and the insurance purchaser is faced with both spatial and temporal basis risks, a temperature,humidity index insurance product would provide risk management benefits to a representative south-central Georgia dairy producer. [source]


Variation in Heat-shock Proteins and Photosynthetic Thermotolerance among Natural Populations of Chenopodium album L. from Contrasting Thermal Environments: Implications for Plant Responses to Global Warming

JOURNAL OF INTEGRATIVE PLANT BIOLOGY, Issue 11 2008
Deepak Barua
Abstract Production of heat-shock proteins (Hsps) is a key adaptation to acute heat stress and will be important in determining plant responses to climate change. Further, intraspecifc variation in Hsps, which will influence species-level response to global warming, has rarely been examined in naturally occurring plants. To understand intraspecific variation in plant Hsps and its relevance to global warming, we examined Hsp content and thermotolerance in five naturally occurring populations of Chenopodium album L. from contrasting thermal environments grown at low and high temperatures. As expected, Hsp accumulation varied between populations, but this was related more to habitat variability than to mean temperature. Unexpectedly, Hsp accumulation decreased with increasing variability of habitat temperatures. Hsp accumulation also decreased with increased experimental growth temperatures. Physiological thermotolerance was partitioned into basal and induced components. As with Hsps, induced thermotolerance decreased with increasing temperature variability. Thus, populations native to the more stressful habitats, or grown at higher temperatures, had lower Hsp levels and induced thermotolerance, suggesting a greater reliance on basal mechanisms for thermotolerance. These results suggest that future global climate change will differentially impact ecotypes within species, possibly by selecting for increased basal versus inducible thermotolerance. [source]


Differential Responses of the Activities of Antioxidant Enzymes to Thermal Stresses between Two Invasive Eupatorium Species in China

JOURNAL OF INTEGRATIVE PLANT BIOLOGY, Issue 4 2008
Ping Lu
Abstract The effect of thermal stress on the antioxidant system was investigated in two invasive plants, Eupatorium adenophorum Spreng. and E. odoratum L. The former is sensitive to high temperature, whereas the latter is sensitive to low temperature. Our aim was to explore the relationship between the response of antioxidant enzymes and temperature in the two invasive weeds with different distribution patterns in China. Plants were transferred from glasshouse to growth chambers at a constant 25 °C for 1 week to acclimatize to the environment. For the heat treatments, temperature was increased stepwise to 30, 35, 38 and finally to 42 °C. For the cold treatments, temperature was decreased stepwise to 20, 15, 10 and finally to 5 °C. Plants were kept in the growth chambers for 24 h at each temperature step. In E. adenophorum, the coordinated increase of the activities of antioxidant enzymes was effective in protecting the plant from the accumulation of active oxygen species (AOS) at low temperature, but the activities of catalase (CAT), guaiacol peroxidase (POD), ascorbate peroxidase (APX), glutathione reductase (GR), and monodehydroascorbate reductase (MDAR) were not accompanied by the increase of superoxide dismutase (SOD) during the heat treatments. As a result, the level of lipid peroxidation in E. adenophorum was higher under heat stress than under cold stress. In E. odoratum, however, the lesser degree of membrane damage, as indicated by low monodehydroascorbate content, and the coordinated increase of the oxygen. Detoxifying enzymes were observed in heat-treated plants, but the antioxidant enzymes were unable to operate in cold stress. This indicates that the plants have a higher capacity for scavenging oxygen radicals in heat stress than in cold stress. The different responses of antioxidant enzymes may be one of the possible mechanisms of the differences in temperature sensitivities of the two plant species. [source]